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. 2023 May 23;7(6):e0166. doi: 10.1097/HC9.0000000000000166

FIGURE 3.

FIGURE 3

DKO mice have more aberrant bile acid metabolism. (A–D) Male WT (n = 5), Tlr5KO (n = 5), FxrKO (n = 16), and DKO (n = 18) mice were aged for 16 months, and liver tissues were harvested for RNA extraction, cDNA synthesis and RT-qPCR for bile acid–related transcripts. (A) De novo synthesis genes i. Cyp7a1, ii. Cyp8b1, iii. Cyp27a1 and iv. Cyp7b1. (B) Bile acid metabolism regulator genes i. Hnf4a, ii. Shp, iii. Fgfr4, and iv. Klb. (C) Basolateral transporter genes i. Slc10a1 and ii. Slco1b2. (D) Canalicular exporter genes i. Abcb11 and ii. Abcb4. (E-G) WT (n = 5), Tlr5KO (n = 5), FxrKO (n = 16), and DKO (n = 18) mice were aged for 16 months, and ileal tissues were harvested for RNA extraction, cDNA synthesis and RT-qPCR for bile acid–related transcripts. (E) Bile acid metabolism regulator gene Fgf15. (F) Apical transporter genes i. Asbt and ii. Fabp6. (G) Basolateral export genes i. Ostα and ii. Ostβ. 36b4 was used as internal control for RT-qPCR. Results are expressed as means ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001. Abbreviations: DKO, double knockout; HNF4α, hepatocyte nuclear factor 4α; Klb, β-Klotho; SHP, small heterodimer partner; WT, wild type.